The term “metabolic syndrome” (MetS) refers to a clus-ter of disorders characterized by central obesity, impairedglucose tolerance, hypertension, and atherogenic dyslipi-demia. Each component of MetS contributes to the progres-sion of heart failure. Proper treatment of MetS reduces thechance of developing heart failure. Optimal management ofMetS in patients with heart failure reduces morbidity andmortality. It is advisable to manage MetS and patients withheart failure with a multidisciplinary team. Future studies areneeded to determine better treatment options for patientswith MetS and heart failure. (1) The pathophysiologic background of myocardial impair-ment in metabolic diseases is multifactorial. Metabolic de-rangements play a central role among a broad spectrum ofputative mechanisms responsible for cardiac structural andfunctional alterations. Predominant changes in cardiomyo-cyte energetics, with a significant reduction in glucose sup-ply and utilization, are associated with the depletion of thesarcolemmal glucose transporter type 4 and with inhibitionof pyruvate dehydrogenase by increased beta-oxidation offree fatty acids (FFA), as well as with tumor necrosis factoralpha–mediated dysfunction of insulin receptors. Direct orindirect effects of hyperglycemia, excess FFA, triglycerideuptake and accumulation in cardiomyocytes, oxidative stress,and insulin resistance (IR) have been widely recognized tocontribute to myocardial alterations in metabolic diseases.The progression of myocardial fibrosis - one of the key mech-anisms underlying cardiac dysfunction is intensified by met-abolic, proinflammatory and neurohormonal factors favor-ing collagen formation, with special contribution from in-creased local angiotensin II, aldosterone, transforminggrowth factor (TGF)-b1, and protein kinase C activity. At thesame time, collagen degradation is reduced by increased gly-cosylation of the lysine residues. Abnormalities of LV dias-tolic performance in preclinical metabolic disease are usuallycharacterized by delayed relaxation, with increased LV fillingpressure being less common. However, the use of conven-tional Doppler for LV filling assessment as well as left atrialenlargement may be somewhat problematic in overweightpatients, in whom the effects of increased loading can be animpediment to adequate interpretation of findings. TissueDoppler imaging is of value in identification of diastolic dys-function in these individuals. The frequency of LV diastolicdysfunction ranges from 23% to 75% in metabolic diseasesdepending on the diagnostic criteria.(14) Insulin resistance and T2DM cause various functional,metabolic, and structural changes, which in turn lead to my-ocardial damage and progression of heart failure. In MetS,activated renin-angiotensin-aldosterone and sympatheticnervous systems can lead to elevated heart rates, renal sodi-um retention, circulating blood volume, ventricular end-di-astolic volume, and cardiac output. Elevated heart rate im-pairs left ventricle (LV) filling and relaxation, increases myo-cardial oxygen consumption, reduces coronary perfusion,and deteriorates LV function. (2).